Health Meaning

After years of fasting Buddha "legs were like bamboo sticks, his spine was like a rope, his chest was as an incomplete roof of a house, his eyes sank in, like stones into a deep well, "according to an account. the Buddha did not get what he wanted from this fast-illumination but a new study suggests that a diet that mimics some effects of milder deprivation can not only reduce your weight but also provide other extreme advantages. researchers report that following the diet for only 5 days per month improves several measures health, including reducing the risk of developing cardiovascular disease.

Eat shortens life, and not just because overindulgence can lead to diseases such as diabetes. a diet to reduce intake food up to 40%, known as caloric restriction increases longevity in a variety of organisms and prevents cancer, heart disease and other diseases of later life. Although some short-term studies suggest that calorie restriction provides metabolic benefits to the people, no one confirmed that it also increases the length of human life. The closest researchers have come from two large long-term studies of monkeys, and they are in conflict as to whether meager rations increase longevity.

Although caloric restriction could add years to our life, almost no one can summon the will to eat so little, day after day, year after year. An alternative could be more, um, acceptable is the fast, temporary abstinence from food. Gerontological researcher Valter Longo of University of Southern California in Los Angeles and colleagues showed that fasting makes the side effects of chemotherapy such as fatigue and weakness, and animal studies suggest that the benefits of this product health similar to caloric restriction.

But fasting core, where people only drink water for days at a time, maybe not easier than calorie restriction. "I did, and it was awful," says Longo. For the new study, he and colleagues designed a less grueling regime could still trigger the benefits of fasting. For two periods of four days each month, middle-aged mice dined low-protein, low-calorie chow. The rest of the month they could nosh much as they wanted.

The mice survived their peers by an average of 3 months, a substantial amount for rodents, and they showed many signs of better health. As the researchers report online today in Cell Metabolism , the mice lost fat and were 45% less likely to suffer from cancer. During their meager episodes kitchen, level of sugar in the blood decreased by 40% and the amount of insulin in the blood was 0% lower. And though the gray matter typically decreases with age, the mice retained more of their mental capacity; they bested control animals in two types of memory tests, perhaps because they produce more new neurons in the hippocampus, a brain area critical for memory.

Longo and his colleagues also have found evidence that the scheme has boosted the capacity of animals to restore and reconstruct tissues. "This is the most exciting" conclusion, says Longo. For example, liver regeneration was faster in fasted animals, and balance of different types of cells in the blood was younger. The number of some stem cells also soared in rodents dieting.

To determine whether the occasional austerity could have the same impact on people, researchers have whipped a menu of energy bars, soups, teas, and fries. The price of a day provides between 725 and 100 calories. "It is not like eating dumplings, but it is better than going without," says Longo. (The average adult man in America needs about 2,000 to 3,000 calories a day ;. following persons calorie restriction can limit to as low as 10 calories)

like mice, study volunteers followed the diet for 5 days straight and returned to their normal food habits for the rest of the month. in their article, the researchers report the results for the first group of 19 subjects to try this diet "imitation fasting" and 19 witnesses.

Only three rounds of alternating between diet and a normal diet seems improve the "fitness participants, reducing blood sugar, trimming abdominal fat, and cut levels of a protein associated with a higher risk of cardiovascular disease. Longo and colleagues also detected a slight increase the abundance of certain stem cells in the blood, suggesting that the diet might promote regeneration in humans. "We believe that fasting is imitating the diet is rejuvenating," says Longo.

Other researchers say the study results are encouraging. "This change in diet can counteract single all these variables of aging, and I think it is very impressive, "says molecular biologist Christopher Hine from the Harvard School of Public Health in Boston. The study shows that cutting calories all the time is not necessary, says biochemist James Mitchell, also of the Harvard School of Public Health. "Intermittent periods can have lasting effects."

The new diet can be more convenient. "Caloric restriction has miserably failed in human trials" because it is so difficult to stick to, said gerontologist Rafael de Cabo of the National Institute on Aging in Baltimore, Maryland, who heads one of the monkey studies calorie restriction. A diet as researchers use "is achievable," he said.

Longo and his colleagues have already completed a larger clinical trial power with more than 80 subjects. Fasting as the Buddha is dangerous, and even fasting imitating the diet could be harmful for some people, such as diabetics, Longo note. Researchers need to study how the diet works, who might benefit and who might be harmed by it, Mitchell notes. "There is a lot of information to understand."

The number of US school children in special education programs because of autism more than tripled between 00 and 2010, to nearly 420,000. But a new study supports a large part of this increase probably came as educators swapped for another diagnosis. The overall percentage of children diagnosed with a collection of brain development problems including autism remained unchanged, suggesting that children who used to be labeled with terms such as "intellectual disability" were actually autistic.

"If you asked me, is it a real increase in the prevalence of autism? Maybe it is, but probably much less than the magnitude reported," said Santhosh Girirajan, a geneticist at the Pennsylvania State University (Penn State), University Park.

in the new study, and Girirajan colleagues combed through data collected in each state for approximately 6.2 million American school children with disabilities who are enrolled in special education programs. The information is collected annually in federal Individuals with Disabilities Education Act. Based on the diagnosis, each child was assigned to one of 13 broader categories, ranging from autism to physical challenges like blindness.

Between 00 and 2010, the number of children in the category of autism more than tripled from 93,624 in 00 to 419,647 a decade later. However, almost two thirds of this increase was associated with a decrease in the rate at which children have been labeled as having a "developmental disability". The number of children in this category increased from 637,270 to 457,478.

The data indicate that the increase in autism is partly the result of students being moved from one category to another, said Girirajan.

for him, the lesson is that autism includes a medley of symptoms. It can also occur in hand with other conditions, including developmental disabilities, epilepsy and hyperactivity disorder attention deficit. This mixture makes it difficult to identify how common autism really is, and lends itself to the development of diagnostics, he said.

The findings, reported today in the American Journal of Medical Genetics Part B: Neuropsychiatric Genetics underline the growing acceptance within the institutions and families a condition, once either ignored or avoided as a mark of shame, says Roy Richard Grinker, an anthropologist at George Washington University in Washington, DC, who has studied rates of autism and wrote a book on autism Minds Unstrange . He points to a recent Washington Post article on the emergence of autistic adults groups pleading for acceptance through events like "Autistic Pride Day."

"Qu ' is this document says is that autism is increasingly adopted as a useful framework acceptable, less stigmatizing, "said Grinker, who has an autistic daughter.

There are certain risk factors that might explain a small amount of the increase in autism, said Jon Baio, a Centers for Disease Control and Prevention (CDC) epidemiologist and lead researcher on a program autism surveillance. This includes children born prematurely or underweight. A recent study in the journal Molecular Psychiatry found that older fathers and older mothers or adolescents had a higher risk of having children with autism.

But Baio, said much of the increase they have seen since 00 has increased awareness of autism and more sensitive screening tools. For example, he said, there are now more cases of autism with milder symptoms, such as normal or above normal intellectual capacity. At the same time, the number of children identified with autism by community experts such as school special education programs examined by the Penn State scientists came close to matching the most complete screening methods CDC.

the possibility that autism figures jumped at children as diagnoses are changed was discussed, said Annette Estes, director of the University of Washington Autism Center in Seattle. The use of wide special education database Penn State study makes a compelling argument that happens, she said. But it does not specify all of the increase. "People who are in the field are generally consensus that the majority of the increase is due to improvements in our ability to diagnose and identify people with autism in a wider spectrum that used to be possible" , Estes said. "But there is that part of an increase not reflected in a number of statistical studies that are made."

* Fixed, July 23 24:09 pm.. the title of this article was changed the original title referred to autism as a disease

There is no shortage of verbiage for vomiting, but surprisingly little is known about the physics behind blowing chunks or how infections spread as a result of regurgitation. previous anecdotal evidence suggested that virus particles specifically norovirus, the leading cause of acute gastroenteritis in the United States could go airborne in-process puke. But according to the food virologist Lee-Ann Jaykus of North Carolina State University in Raleigh, "no one has ever proved in a laboratory model that the virus can be aerosolized by vomiting." To remedy this, Jaykus and his team built a miniature "machine vomiting," quarter-scale model of the entire human digestive system with an artificial stomach, esophagus and mouth. They designed to mimic all the pressures and volumes present in humans hurling then inoculated his juice "stomach" by a virus called MS2 (which is similar in size, shape and composition of norovirus but not dangerous to humans). They ran the machine in a sealed chamber connected to a sensor capable of detecting all floating virus particles. The team reports today in PLOS ONE , used a variety of different pressures, vomit viscosities, volumes and concentrations of virus and found that in every instance-MS2 viral particles can be detected in the air. As expected, more virus particles were aerosolized MS2 when more was added to the stomach and at the same time the viscosity of vomiting and the system pressure were found to be important variables. Most virus-over 13,000 particles were observed with the concentration of the high initial virus and high viscosity of vomit. According to the team, the results confirm the plausibility of anecdotal reports of norovirus is transmitted through the air after a round of retching.

ravaged countries Ebola West Africa are on alert after a polio case was confirmed in a young child in Mali on 7 September, just a week after two cases were reported in south-western Ukraine. The homes are not related, but in both cases, the culprit is supposedly derived poliovirus vaccine (VDPV). These rare VDPV occur when the virus used in the live vaccine returns from its weakened form and regain its virulence danger when immunization rates are low because they are in two places, allowing the vaccine strain circulating and accumulate genetic mutations.

in West Africa, a boy of 19 months, was paralyzed in Guinea on 20 July, then went to the Malian capital for treatment, where polio was confirmed. Type 2 VDPV is closely linked to that detected in the Kankan Region of Guinea in 2014 that researchers believe was undetected circulation for 2 years. Because the West African health systems have been decimated and vaccination rates dropped precipitiously, the World Health Organization (WHO) estimates the high risk of spreading.

Ukraine, with its social unrest and declining child vaccination, approximately 50% of children were unemployed or underimmunized in 2014-was also considered as high risk of a polio epidemic. Two children there, 4 years and 10 months, were paralyzed June 30 and July 7, respectively; Type 1 VDPV was confirmed August 31 The risk of spread in Ukraine is high, the WHO said, although the risk of international spread is low.

Both homes Polio is so contagious that one case is considered an outbreak underscore the urgency for all countries to stop the use of live oral vaccine, a key strategy in the final phase of polio eradication, said Hamid Jafari, head of global polio eradication at wHO in Geneva, Switzerland. For now, if a wild virus or vaccine derived causes an epidemic, the answer is the same: Hit the area hard and fast with massive vaccination round and cancel within 4 months. Emergency campaigns could begin this week.

Still a brilliant victory in the battle of the drug against the hepatitis C liver damaging virus (HCV) may be on the horizon: A small study suggests it may be possible to cure some people of their infection in as little as three weeks.

fresh on the heels of recent approvals of four new combinations of HCV drugs that clear infection from many different types of viruses in about 3 months, a team led by George Lau hepatologist humanity and healthy GI and liver Centre in Hong Kong, China, has mixed and matched various compounds to see if they could still shorten the road to recovery. After 3 weeks of treatment, 18 HCV-infected persons given three different drug combinations met the standard definition being cured at 12 weeks after starting treatment, they had no signs of genetic material of HCV RNA in their blood on standard tests. The researchers plan to present these data to the public for the first time at a scientific conference known as The Liver Meeting in 2 weeks.

Until new drugs for HCV have appeared, infected people needing treatment for 8 months, as well as therapies often fail and had serious side effects. Now the standard treatment protocol calls for HCV drugs taken for only 12 weeks. Cut that time even more dramatic treatment is "really, really fascinating," said Shyam Kottilil, an HCV researcher at the Institute of Human Virology in Baltimore, Maryland. And if the results are valid, it could reduce the cost global processing $ 100,000 required by the most popular drugs used for the treatment of 12 weeks. Kottilil own study of a treatment four weeks tested different drug combinations on a single a different rate of population patients were 40% healing in 50 participants. (This study is in press in Annals of Internal Medicine.)

other researchers point out several warnings to the success of three weeks including the 18 people treated had several characteristics of patients who respond well to HCV drugs. "It is very interesting, but not unexpected," said David Nelson, a researcher of hepatitis at the University of Florida in Gainesville.

Raymond Schinazi, a biochemist at Emory University in Atlanta, who worked with Lau, recognizes that this is only a pilot study and needs confirmation in a larger clinical trial. "But when you get 100%, it is still statistically significant," said Schinazi, who helped develop a new blockbuster drugs HCV sofosbuvir, which was part of the combinations tried in the new study.

the rapid clearance of HCV from the body seen in the study upends mechanistic models of how the treatment heals people with HCV. "Our models do not predict at all," said another employee, Alan Perelson, a biophysicist Los Alamos National laboratory in New Mexico, which has an essential work on how the treatment led to the clearance of HCV and HIV. "There is a piece of basic science on viral clearance we are still missing. "

Until May 2011, the only drugs approved to treat HCV worked by non-specific disorders and antiviral and immune mechanisms, have significant side effects, and 40% of the time. Since then, a dozen so-called antivirals direct action came on the market, all of which are expensive and many alike, promising candidates are in development.

The study of Hong Kong tested three different triple combinations of antivirals most effective direct action, each of the houses on different HCV enzymes or proteins important for replication. Sofosbuvir-created by a small biotech Schinazi began which was acquired by Gilead Sciences of Foster City, HCV polymerase California target RNA and was the backbone of all three regimes. Widely regarded as the "first in class" in the world of HCV drugs, sofosbuvir has a relatively high power, causes few side effects, and is rarely thwarted by drug resistance mutations. (Its selling price initial retail, $ 1000 per pill, sparked an international controversy.) the researchers combined with either ledipasvir or Daclatasvir, paralyzing a viral protein known as NS5a. To finish the cocktail, the researchers added one of two inhibitors of HCV protease, Simeprevir or Asunaprevir.

Three different companies Big Pharma are various medications, and Schinazi says that to protect their markets, they resisted to collaborate with each other. "I want to show these companies they should have done this long ago study themselves, "said Schinazi, which helped pay for the drugs used in the study." When you put together the best drugs, you get fabulous results . "

to achieve these results, the researchers deliberately have the lowest hanging fruit and Hong Kong was an ideal test site. HCV has six genotypes which are, in turn, are divided into subtypes. In China, the most common is the genotype 1b, responding more readily to drug treatment than any other genotype: Previous studies have shown that 8 weeks of sofosbuvir ledipasvir and can cure almost everyone. Large studies have also found that 84% of patients with HCV Chinese have a variation of an immune gene (technically known as IL28B cc ) which leads to a strong natural attack against the virus in giving them an advantage when treated with effective drugs. "So you're looking at [a] population that has not only the best genotype, but the host may play a role," says Mark Sulkowski, director of the center of viral hepatitis at the Johns Hopkins University School of Medicine in Baltimore, Maryland.

investigators stacked the deck in two other ways. As is commonly done in clinical trials of HCV drugs, they excluded people infected with HCV who underwent liver cirrhosis and therefore are more difficult to cure. in addition, the study used an unusual guided study model called response therapy. a total of 26 persons started treatment and the researchers checked their blood levels of HCV after 2 days the selection of 18 people who had larger viral load decreases to the short duration of therapy and treatment of other standards for 12 weeks. These 18 participants were also lower HCV viral loads pre-treatment.

The University of David Nelson of Florida said the study "is a great proof of concept", but wondered how applicable the 3-week treatment system will be in the global response. Although the genotype 1 accounts for approximately 46% of all infections worldwide, the majority of Americans subtype 1a-more difficult to treat. about 22% of people have the genotype 3, which is similar more difficult to cure as 1b. Ideally, said Nelson, a standard treatment protocol should work against all genotypes without the need to test the initial responses and whatever the status of cirrhosis.

Although Sulkowski accept that treatment ultrashort will not be a single one-size everything, he replies that it can be pragmatic in certain contexts. "This study really opens up a philosophical discussion on how to treat hepatitis C," says Sulkowski. "Maybe it there is a role for a complicated strategy that shortens the therapy. "in the US, for example, it may make economic sense in some health care systems to pay extra to test genotype 1b patients-representing 25 % of the population infected two days in therapy and selecting speakers for the treatment course of 3 weeks. Consider that nearly 180,000 people who receive care from the Veterans Health Administration have tested positive for HCV: According to estimates, it would cost $ 12 billion to treat everyone for 12 weeks, even the greatly reduced in rate for drugs. Shaving 9 weeks for thousands of people could equal huge savings in drug costs.

Sulkowski said although the ultrashort therapy regimen does not have a cure rate of 100%, it may not pose great risks for patients. As he and others reveal at the liver meeting a growing body of evidence shows that patients who fail to treatment often respond if treated again with different drugs. "If I tell a patient, I'll treat you for 4 weeks and if you do not answer, I can save you with another approach, which is a reasonable strategy for a country like the United States"

Schinazi said combinations of more powerful drugs and higher doses of existing ones could reduce the time to heal further. "I think eventually we could go to 2 weeks," he said.

Parasitic worms bored into our bodies, steal our nutrients, and sup on our blood, but their effects are not all harmful. A new study of people living in the Amazon suggests that certain intestinal worms increase the number of babies women give birth to.

"This is a very original study," said Rick Maizels parasite immunologist from the University of Edinburgh, who was not connected to the research. "I think this will spark many more inquiries" about the impact of breeding worms.

More than 1 billion people are infected with intestinal worms, mainly in tropical areas with poor sanitation. One of the most common is the giant roundworm Ascaris lumbricoides , which can reach 36 centimeters (14 inches) in length. roundworms giants reside in the small intestine and the sliding of a portion of food from their host. Other worms, such as hookworm Ancylostoma duodenale and Necator americanus , are tiny vampires. They puncture the lining of the intestine and drink the blood of their host.

For all their bad habits and icky, parasites have much in common with a fetus in the womb. The immune system provides a parasite and a fetus as intruders, so both need strategies to support what researchers called immune tolerance. Parasites can cause some of the same immune changes that occur during pregnancy example for the stimulation of regulatory T cells that mater immune attacks.

Because of these similarities, human biologist Aaron Blackwell of the University of California, Santa Barbara, and colleagues wondered whether parasitic infections could open the way to pregnancy. The researchers attempted to answer the question by analyzing data on Tsimane people living in the Amazon rainforest of Bolivia.

The approximately 16,000 Tsimane survive mainly by hunting, fishing and the cultivation of plants such as rice and plantains. Their homeland is first parasitic country. About 15% to 20% of them are home Ascaris , and 56% of them carry hookworms. Infected women in the study were generally not aware they were playing the host of parasites, says Blackwell.

The only health effects researchers were able to detect in almost 1,000 women were Tsimane in individuals carrying hookworms. They had a slightly lower body mass index and lower levels of the protein hemoglobin that carries oxygen in the blood. Hookworms were also detrimental to fertility. They increased the age at which women first gave birth Tsimane and stretched the amount of time between pregnancies. As a result, the team calculated a woman with hookworm would three fewer children in his life than would a woman devoid of parasites. For Tsimane women overall, however, fertility is not a problem because they give birth to an average of nine children.

In contrast, the giant roundworm Ascaris was a godsend for reproduction. It shortened the time between pregnancies and reduces the age at which women give birth first. A woman infected with Ascaris would average two other children in his life than would a free woman parasites, the researchers report online today in Science . "It is somewhat intuitive-cons," says Blackwell.

By tweaking the immune system, Ascaris to reduce inflammation and therefore could promote the design and implementation of the embryo in the womb, the team speculates. Hookworms, however, are not as good for inhibiting inflammation, and suck their blood and nutrients fly could overwhelm the benefits of reproduction they provide, the researchers suggest. Blackwell and her colleagues are currently analyzing women's blood samples to determine which cells and immune molecules to change.

other studies have shown that living bacteria in our body are essential for pregnancy, reproductive immunologist notes Gil Mor at Yale School of Medicine. But the idea that "the worms can affect reproduction, even improving reproduction is quite surprising," said -he. The study highlights the fact that "the state of the immune system is of crucial importance for successful reproduction," says Norbert Gleicher, a reproductive immunologist at Rockefeller University in New York.

Because immune changes triggered by parasites can remove allergy, asthma and autoimmune diseases, several clinical trials have tested whether people infected with worms soothes the symptoms of these conditions. Researchers suspect that Ascaris will never become a treatment of infertility, however. "I would never give my patients that parasite," says Mor. But the results could still lead to new therapies, said Gleicher. "If this [finding] is true, we could develop an immunization that produces the same kind of immune response as does the roundworm infection."

At its peak, the Roman Empire spanned three continents surrounded the Mediterranean, and was the home of a fifth of the population of the planet. The Romans brought roads, bridges, and, perhaps most importantly, sanitation. But a new study of ancient feces casts doubt on how effective the Roman sewage system was to improve public health.

"I think it's a good piece of work," says Jürg Utzinger, an epidemiologist at the University of Basel in Switzerland, who was not involved in the study. "It is not a easy task, because we are talking of the review feces dating back thousands of years ago. "

For sanitation, the Roman Empire seemed to do much good: There were public bathing facilities, public toilets, and orders dictating how the waste should be disposed. Rome itself had an impressive sewer system-famous aqueducts. "In the Roman Empire, where they improved sanitation, I would have expected some decline in parasitic infections," says Utzinger.

But that is not what the new study. Piers Mitchell, a paleontologist at the University of Cambridge in the UK, combed through previous studies of more than 50 archaeological sites around the Mediterranean to get an idea of ​​what the parasites were living in and on humans before and after the Romans took over. Many of these studies relied on microscopes and chemical tests or DNA to detect parasites and their eggs in the soil from tanks and public latrines. Mitchell has focused its analysis on these sites because they contained fossilized dung, called coprolites, which can keep eggs of parasites and DNA for thousands of years. Using this evidence, he described the geographic extent of several parasites.

Despite technology sanitation Romans, Mitchell found that intestinal parasites like whipworms ( Trichuris trichiura ), roundworm ( Ascaris lumbricoides ) and Entamoeba histolytica (the causative agent of dysentery) increased in areas after the Romans showed up. He says he was surprised at first, but believes that the increases actually have logical explanations.

Although the Romans were at the forefront of sanitation technology, they do not yet understand the germ theory and they do not know much about parasites, either. Historical documents show that farmers used human waste collected in the cities to fertilize their crops. Parasite eggs can stay alive in feces for a long time and, according to Mitchell, the practice could easily have contributed to the success of the roundworm.

Moreover, Ann Olga Koloski-Ostrow, self-professed "Queen of latrines" and a classical archaeologist at Brandeis University in Waltham, Massachusetts, who was not involved in the study says it is difficult to know exactly what is the prevalence of the use of human excrement as fertilizer was actually during the Roman Empire: "We can only say that in some texts on agriculture early we know that they build the slave toilets to an area where feces could be collected and spread on crops, but that was just on isolated farms here and there. "However it also notes that many Romans, without access to sewer systems used inside emptying toilets also often located just off the kitchen. That waste was used as fertilizer, she said, it is easy to see how parasites could have ended up in food.

the new study also identifies saunas as a potential hotspot of disease. Although the Romans designed to promote cleanliness, most installations were badly maintained and the water was allowed to grow dirty-acquisition of a "scum on the surface of dirt and human cosmetics," writes Mitchell. The hot and humid environment may have provided an ideal breeding ground for parasites.

Mitchell's analysis, published online today in Parasitology , also shows that the Roman Empire often spread tapeworms of fish in the conquered regions. "They are about 20 to 25 feet long, and they wrap around the inside of your intestines. People get them from eating raw or undercooked fish," he says. The Romans many cooked foods, but they have also fostered a sauce called garum, which is made by fermenting fish pieces and various seasonings under the hot sun. Because the sauce is never heated, Mitchell postulated that it may have been an ideal vector for the spread of tapeworm eggs fish around the empire. As the empire expanded, it brought along its culinary culture and its parasites.

The new analysis also shows that the head and pubic lice were common throughout the empire, as well as fleas and bedbugs.

But despite all this, Koloski-Ostrow said it would be a mistake to write off the Romans as a dirty or disgusting society. Many of their ideas, such as fertilizers and saunas were fundamentally sound, but just missed the mark in terms of performance because they simply did not understand how germs and parasites were distributed, she said . "You can not blame the Romans for that. It is something they are not honestly aware of"

Fixed, January 8, 11:15 :. This story was corrected to reflect this reasearch was published in Parasitology instead of The American Journal of Parasitology .

As Fear of Zika virus spread almost as quickly as the pathogen itself, two new laboratory studies provide the first strong evidence for how it could cause brain defects in babies: the virus appears to preferentially kill cells of the developing brain. The observation reinforces the case more and more for a connection between the virus, which is spreading rapidly throughout Latin America, and an increased number of cases of microcephaly, a birth defect in which the brain fails to develop properly. The new work, performed independently by two groups, indicating that the virus infects cells easily neural stem precursors to neurons and other brain cells if they are grown on cell culture plates or coaxed to form minibrains 3D brain called organelles.

work "will be very important," said Madeline Lancaster, a developmental biologist who studies human brain development in molecular biology research laboratory in Cambridge Medical Council, UK results "are all in line with what you see babies with microcephaly. "

Zika virus, named after a forest in Uganda where there are first isolated decades, usually causes only mild symptoms in people including fever and rash. But after the virus began spreading in northern Brazil last year, the doctors, he noticed a striking increase in the number of babies born with microcephaly. most mothers reported symptoms consistent with Zika infection during their pregnancy. But it has been difficult to prove a link between the virus and birth defects because blood tests for Zika virus are accurate for about a week after 'infection.

However, circumstantial evidence has accumulated. The researchers identified the virus in the amniotic fluid of pregnant women whose fetuses were diagnosed with microcephaly and also in the brain tissue of a fetus diagnosed with the disease. But because researchers have researched little about the virus before this year, they had little data to suggest how the virus could cause such damage.

To evaluate the possible effects of the virus on brain development, researchers from Johns Hopkins University in Baltimore, Maryland, and Florida State University in Tallahassee he used stem (iPS) cells induced pluripotent cells to develop in laboratory dishes, the immature brain cells called progenitor human neural cortex. (IPS cells are adult cells that have been reprogrammed into stem cells that can develop into most tissues in the body.) They then exposed neural progenitor cells in a laboratory strain of virus Zika.

The virus easily infected neural stem cells, neuroscientists Hongjun Song and Guo-li Ming, virologist Hengli Tang and their colleagues report today in Cell Stem Cell. Three days after the virus has been applied, 85% of the cells in culture dishes were infected. However, when the virus was applied to the fetal cell cultures of kidney, embryonic stem cells and undifferentiated iPS cells were infected within 10% of the cells by day 3. The immature neurons derived from neural progenitors are also less sensitive to the virus; 3 days after receiving a dose of the virus, less than 20% of these cells were infected.

The researchers found that progenitor cells infected are not killed immediately. Instead, the virus "hijacked cells," using the cellular machinery to replicate, said Song. This allowed the virus to spread rapidly through the cell population, he said. His team also reported that the infected cells grew more slowly and disrupted cell division cycles, which could also contribute to microcephaly.

In a separate set of experiments, other researchers found that the virus can hinder the growth of another type of neural stem cells. In a preprint posted March 2, neuroscientist Patricia Garcez and stem cell researcher at the Stevens Rehen D'Or Institute for Research and Education in Rio de Janeiro, Brazil, report more human iPS cells in clusters of neural stem cells called neurospheres, as well as 3D organelles that in some ways resemble a miniature version of the human brain. When they infected the cells with growth isolated Zika of a Brazilian patient, the virus quickly killed most of neurospheres and left the few survivors and misshapen. organelles infected grew at less than half of their normal size.

Lancaster said the findings echo previous studies of genetic mutations that cause microcephaly, which also affect neural progenitor cells. "You have two very different causes of microcephaly, but you know something is happening very similar: a depletion of neural stem cells, and that would lead to fewer neurons" in the brain development, she said

Many questions. on the Zika virus and its apparent link with birth defects remain unanswered. both Garcez Song and say they are now repeating their experience with other viruses, including dengue, a virus closely related to Zika prevailing in the regions currently affected by the epidemic. (Some scientists suspect that prior exposure to other viruses might affect the outcome of Zika infections.) the researchers also still need to understand how the virus crosses placenta and infects the fetus directly, that most viruses can not do.

More:

• Therapy gene gets a high-stakes test

at the time of his birth, 41 years ago in Germany, Oliver Semler had already broken a bone, a thin pencil rib. This, arched his femurs, and a second fracture at the age of two days doctors said he had osteogenesis imperfecta (OI), a debilitating genetic disease that makes bones fragile and often break easily being pushed to school, for example, or slipping on wet leaves outside. Or, as in the case of Semler, acrobatics in the uterus. "I had a cast two or three times a year," said Semler, who lost many of its fractures, but has undergone 27 surgeries to repair the worst of them. "To my colleagues at school, it was normal. Oliver is not there 2 or 3 days, and he returned to school with a cast."

We have to do a clinical trial before people are willy-nilly.

improbably, given the severity of his illness, Semler avoided life in a wheelchair, but its growth was slowed and he stands 4 feet 8 inches tall. He attended medical school and became a pediatrician at the University of Cologne in Germany, where he takes care of 250 children with his condition. Semler is now preparing for the first time in OI and beyond :. A clinical trial of a stem cell treatment for the afflicted fetus, which aims to give them a better start in life than himself had

The trial, still being planned, is one of a handle being designed in Europe and the US to perhaps the most difficult patient population, it is: pregnant women and their fetuses. After decades of dashed hopes raised and, paediatricians, immunologists, and others are cautiously hoping that new biological knowledge and a push for treating parent-to-be could reverse the trend of stem cell therapy prenatal. "I think [there’s] much of an understanding of what is possible, what is safe, what is ethical," says Anna David, who studies fetal therapy at University College London and collaborates with Semler on the trial of OI.

Even the tests with only 30 or so mothers, the target for the study of OI require Herculean effort: a dozen academic partners and industry, dozens of doctors, million . A high-profile failure or worse, an injury to the mother or fetus, could define the decades field. "That's what keeps me awake at night," said David. "Security, trying to tick all the boxes, thinking as much as possible" on everything that could go wrong. Some fetuses have been treated on an ad hoc basis, with encouraging results, and it is a stimulating factor trials. But then is the probability that a bottle of good cells, administered at the right time, could stop a devastating disease before birth.

In the 1980s, when Semler was in elementary school, hopes ran high for the fetus treatment with stem cells. Because the immune system of the fetus is still in development and some of his guards, such as T cells, are not fully functional, doctors believed that the fetus would easily accept cells unlike abroad, even a baby, who may need chemotherapy or other toxic treatments to suppress the immune system. The transplanted cells would grow into healthy blood cells, immune cells, or other fetal parts were missing, thought has therefore stop the damage that a disease has already been inflicted in the womb. Maria Grazia Roncarolo, then a young pediatric immunologist, recalls the heady days in Lyon, France, where this theory was put to the test.

In 1988 and 1989 the Hôpital Edouard Herriot, two fetuses whose blood cell markers showed they had serious immune disorders became the first to receive a transplant of cells. Doctors led by Jean-Louis Touraine infused through the umbilical vein with blood stem cells from 7 to 10 weeks of age aborted fetuses. Roncarolo helped supervise the first baby after birth. With a little boy squirming in front of her, "I'm really totally excited," she said. "I thought I found a way to cure all genetic diseases. My young complete naivety, I thought I had found a solution."

A third fetus everyone on Earth. Instead of an immune deficiency, he had thalassemia, a disease potentially fatal blood. Hoping to treat the fetus when his immune system was particularly primitive and disease at a nascent stage, the doctors infused stem cells into the abdominal cavity of the fetus at 12 gestational weeks. In their defense, the cells were rejected and the transplant failed.

"The assumption that we had that the fetus was tolerant [of foreign cells] was wrong," said Roncarolo. Brutally disappointed, she revamped her career, returned to basic research and now works at the University Stanford in Palo Alto, California, where she is studying stem cell transplant and immune tolerance. Meanwhile, the rest of the Lyon team persevered, but the results were disappointing. Two fetuses died before birth of the treatment. in two other cells-all of aborted fetuses-graft didnt at that time, doctors stopped their efforts

Externally, the interest in stem cell therapy for fetal faded. . But behind the scenes, a small cohort of researchers undertook a trip many years to understand why it did not work when immunology suggested he should. pregnancy is a unique, two genetically distinct beings that intertwine without rejecting the other-a framework that, at least in theory, should provide an opening for cell therapy.

In the late 00s came a string of discoveries that helped explain the successes and failures. For one, researchers learned that fetal T cells are actually able to reject the invaders if a microbe or transplantation of cells more easily than foreign thought. Later, other researchers have found that it is probably not only the fetus which had condemned these grafts anterior cells. maternal immune cells are inevitably flow through the fetus, and in the mouse studies, these cells have rebelled against the donor cells.

A group led by Mike McCune at the University of California, San Francisco (UCSF), however, found an encouraging phenomenon: Some of fetal T cells are primed T cells to convert regulators supposedly which can tolerate foreigners, especially the cells of the mother. In mice, "if you match the graft mom, [nearly] all fetuses that you can transplant graft," said Tippi MacKenzie, pediatric surgeon at UCSF. She began to wonder if cells mother donor could be the most likely to be accepted. "it was the eureka moment," she said.

Mackenzie and others have also found that in animals, higher doses of donor maternal cells were more effective, and inject them into the blood of over increased success fetus. In humans, this becomes possible after gestation of 18 weeks, channeling the cells through the umbilical vein.

drastic solutions As science plugged along, desperate parents sought. In early 02, Madeleine and Stefan Karlsson, living in Uppsala, Sweden, and pregnant with their first child were a rollercoaster of uncertainty. An ultrasound at 20 weeks had raised red flags, but additional tests implemented anything. At 25 weeks, doctors "have discovered that something is wrong," recalls Stefan Karlsson. "After that, we have ultrasounds every week, and next week everything was fine, and the week after that something wrong again, but nobody knew what. "at 30 weeks gestation, a little more than 2 months before normal delivery- doctors shipped out fetal cells for analysis. The results were devastating. The Karlssons learned that their daughter had OI, later diagnosed as the most severe form of type III. only one other child in the world, Canada has been identified by the same mutation. the baby died at the age of 5 months.

the Karlssons were referred to the Karolinska university hospital in Stockholm, where doctors suggested a radical strategy: the harvest of a specific type of stem cells from the liver of an aborted fetus and infuse through the vein umbilical in the fetus that Madeleine was wearing. The family agreed.

"We have transplanted about 6 million cells," says Cecilia Götherström Karolinska, which produced the cells. The stem cells used, mesenchymal stem cells (MSCs), are supposed to cause less vigorous immune response that the blood stem cells, mesenchymal stem cells can grow into bone, and other connective tissues. the hope was that MSCs would take hold and
produce new healthy bone.

the transplanted cells are a genetic match to the mother or fetus, the Karlssons appoint Olivia Nevertheless, at least some of them grafted. When Olivia was 9 months the cells of the donor biopsy revealed a mixed bone with its own

at first, Olivia did better than expected .. But doctors around his sixth birthday, she began to deteriorate and suffered a series of fractures. Finally, Götherström Olivia and her colleagues transplanted back more MSCs from the same donor tissue. Fractures Olivia diminished, and it was transplanted back every 4 years since. Now aged 14, she has not had a fracture in 18 months, surprising his doctors. The father of Olivia, she said swimming for physical therapy, enjoys sewing, arts and crafts, and like most teenagers, clothing stores and spending time with his friends.

Götherström knows that without a control group, there is no way to be sure that MSCs helped Olivia. However, encouraged by the Olivia experience, she and her colleagues later fetal MSCs shipped to Singapore for further treatment of a fetus with OI and infused a third of parents traveled to Sweden their home in Ireland; this child is now a toddler. And, with others, Götherström began to lay the foundation to see if in utero therapy was really made a difference. "We have to do a clinical trial before people are willy-nilly," said David UK, particularly because interest in such treatments may increase as it becomes easier to diagnose serious problems in utero.

There are two years, and Semler Götherström met at a conference on OI in Wilmington, Delaware. stem cells Until then transplanted Semler had not considered a viable treatment for the disorder. But he knew better than almost everyone that severe OI stand before birth, when the skeleton is still in training. On ultrasound, doctors detect shortened leg bones and even fractures. MSCs supply as soon as possible, Semler thought, could give a fetus a better chance to build healthy bone without the side effects of a bone marrow transplant after birth. And Götherström thought infusing the cells before birth had a better chance of working in part due to differences in the fetal circulation: The cells infused into the bloodstream are less likely to get stuck in the lungs and never surrender to their destination than they are in a baby.

A test of OI, called BOOSTB4, now sharpens towards the starting line. Götherström, David, Semler, and others have obtained more than $ 9 million from the European Union and the Swedish Research Council, and are developing their protocol. Starting later this year, they hope to begin recruiting 15 families across Europe with fetuses made by ultrasound and DNA tests have severe OI and in the second or third quarter infuse with MSCS from liver cells fetal, like those received Olivia. Infants receive additional infusions after birth. They will be compared to another cohort of 15, who will receive the MSC transplantation after birth, and with historical controls. All children will be followed for 10 years, to see if those treated in utero and after fewer fractures, better bone density, improved growth and better quality of life.

"We are not aiming for a cure," warns Götherström. "It is not that they will raise a wheelchair and start running." Instead, she hopes to halve the number of fractures, which with the safety demonstration, is the objective of the test, make a big difference for patients and families. and just snatch a trial like this "could open a wider range of other conditions treated" before birth, she said.

in the US, the group of Mackenzie and another took a different approach: the treatment of fetus with blood stem cells taken from their mothers, the strategy it began exploring animals there are nearly a decade. last month, it filed an application with the US Food and Drug Administration to provide hematopoietic stem cells to the fetus with α-thalassemia, a severe form of the disease that is fatal before or shortly after birth. the prenatal cell therapy failed for thalassemia there nearly 30 years, but Mackenzie hopes a different outcome this time.

Because the cells come from the mother, she expects them to be better tolerated and infuse a much higher rate in the umbilical vein after gestation of 18 weeks. "If this process does not work, then we would go earlier," said Mackenzie, potentially injecting the cells into the fetal heart.

Alan Flake at the Philadelphia Children's Hospital (CHOP) in Pennsylvania is planning a similar trial of maternal stem cells in fetuses with sickle cell anemia, a painful debilitating disease that often reduces the life. (Flake led the transplant of fetal stem cells only known in the United States. made in the mid-190s on a fetus with severe immune deficiency, he has used stem cells from the donor by the father, and was considered largely successful.) Flake refused to speak with science citing a busy schedule and concerns about hyping a yet treatment in the trials, but in a video on the CHOP website he was optimistic. "the results of the research are absolutely convincing that we can achieve a healing sickle cell disease, "said Flake. The hospital raises millions of dollars to support a trial.

The medical risks of cell transplants in utero are generally considered modest, but include loss of pregnancy. Similar procedures such as fetal blood transfusions for anemia, are already available. But some fear the risk that may come after birth. "We rely on the idea that stem cells proliferate and differentiate into what we want," said David Chitayat, a medical geneticist at the Hospital for Sick Children in Toronto, Canada. Chitayat questions whether the proliferation may proceed unexpectedly, for example leading to tumors, a concern that cuts across many stem cell therapies. (Mackenzie notes that it should not be a problem for the strategy, because it plans to use the same type of cells than bone marrow transplants, which are not due to tumors.)

There are also concerns that the mother will be encompassed by the interests of the fetus, especially the fetal treatment programs are generally based in children's hospitals, and pediatricians consider the fetus their patient. "There is a person who has this uterus in her body" to be consulted, said Anne Drapkin Lyerly, a bioethicist at the University of Carolina North, Chapel Hill, who studied fetal surgery for spina bifida and other conditions. Any treatment will not only affect the fetus, but "the people who will be taking care of this baby," she said. Lyerly admits she does not know exactly how these concerns should be addressed beyond a particular attention to experience of the mother, including how it can react if the treatment results in pregnancy loss.

the doctors to conduct these tests are fully aware of the risks but emphasizes that the conditions they intended to treat cause suffering in life and often early death. If prenatal stem cell therapy is effective and safe, ethicists and other doctors agree, it could change lives. and as Chitayat rating, " if you do not start, you do not know. "

Sharing why he embraced cell therapy 14 years ago, when his wife was 7 months pregnant and the far field murkier it is today, Stefan Karlsson reached a response any parent can appreciate. "For us it was we see no disadvantages to try stem cells, there were only benefits," says. "And it might help to Olivia."

Pharmaceutical giant AstraZeneca joins several heavyweights in the genetic sequencing to mine up to 2 million people genomes for new drug targets. The London-based company, today launched a genomic internal center that exchange data and samples with Human Longevity Inc. (HLI) -geneticist ambitious Genomics J. Craig Venter startup and integrate a research team from the Wellcome Trust Sanger Institute in the UK. The Company expects the entire genomes, combined with data on individual health, reveal rare genetic variants that influence the disease and suggests new drug targets.

Given that only about 100,000 people worldwide had their whole genomes sequenced to date, the new resource would be unprecedented, says geneticist Eric Topol of the Scripps Research Institute in San Diego, California, which is not involved in the partnership. Other pharmaceutical companies have made large investments in genomic data. 2012 Amgen repurchase of 140,000 volunteer base data deCODE Genetics was "somewhat of a precursor to this," Topol said, but it was limited to Icelandic population and did not include whole genomes for each participant. "This is about finally getting some power for us the big data, the level of the entire genome," he said.

Many in the hope of such power will revive a field field that promised more than a decade to find drugs based on disease-causing mutations. "I think we need to be clear and admit that the fulfillment of these promises has taken much longer than many people expected," said David Goldstein , a human geneticist at Columbia University and scientific consultant to AstraZeneca, in a press conference today. "I really personally believe that we finally ... a turning point."

Under the arrangement, HLI will sequence an anticipated 500,000 samples of participants in clinical trials from AstraZeneca, and share his own collection million expected genome. (Venter said the company already has 26,000 complete genomes with corresponding clinical data, and adds approximately every 15 minutes.) Without large databases of whole genomes or exomes, the portion encoding the protein genome, looking for drug targets has so far found that common variants with little effect on the disease, and genetic research has "used his tools," he said. "It is the rare variants in each of us who determine our traits."

The partnership also includes the University Institute for Molecular Medicine Finland Helsinki, which will provide for the analysis of thousands of genomes and samples sequenced from its biobank, accompanied by songs compiled in the country's health care system. AstraZeneca researchers can choose a gene of interest and research of the Finnish population for variants associated with diseases, or to identify specific safety concerns in the treatment of patients with a given mutation.

Meanwhile, AstraZeneca plans to convene a scientific team based at the Sanger Institute and led by one of its employees, to identify drug targets from its data. As Sanger Institute director Mike Stratton explained at the press conference today, the new team will "walk the halls of AstraZeneca" and " open the doors between the two intellectual worlds. "

This cozy arrangement might prove complicated for the institute, said Eric Campbell, a sociologist who studies the relationship between universities and industry at Harvard University. "Relations industry have helpful benefits ... but the risks are great for an institution," he said. He wondered whether the presence of the AstraZeneca will move research to drug discovery projects of mind of the Sanger Institute, for example, and if researchers will be free to publish results that show damage or risks potential of AstraZeneca products.

AstraZeneca did not disclose financial details of the agreement, but Venter revealed in a closing comment that the arrangement had taken a year of negotiations: "You make babies faster than you. can do a collaboration of the genome "

Earlier this month, U.K. mountaineer Richard Parks prematurely abandoned the expedition team to the summit of Mount Everest in Nepal. He planned to ascend the summit without supplemental oxygen in the Everest Cynllun project and take the highest elevation blood sample and muscle biopsy ever assembled. initial objective was to examine the relationship between hypoxia and cognitive decline by examining the human performance in oxygen deficient environments, but its abrupt end raised questions of another kind.

The team had for several weeks been climbing smaller peaks to acclimatize to the high altitude, and Parks was about to begin its second rotation of the mountain: a 2 week stay above the Khumbu Icefall (5486 meters). Damian Bailey, a physiologist at the University of South Wales in the United Kingdom and the Chief Scientist of the project, decided to carry out a blood test on earlier than planned parks. When he drew blood, he immediately knew something was wrong. "His blood was extraordinarily thick," Bailey said. "It was actually bleeding as I was taking a sample."

The tests revealed that Parks had unusually high levels of red blood cells and a high hematocrit, . the percentage of the mass of the blood composed of red blood cells one hand, it was an index of the ability of Parks to operate in conditions of low oxygen, "His brain was actually getting more oxygen than this would get at sea level, "Bailey said, despite the thin alpine atmosphere containing half the amount of oxygen found at low altitude. But these high cell densities also the start to an increased risk of stroke brain or heart attack. for this reason, the team decided to end the expedition on 3 May, despite seeming Parks outward in perfect health.

the same project managed to collect data for its original purpose to examine the relationship between hypoxia and cognitive decline. In addition, Bailey hopes to schedule a follow-up expedition at some point. But for now, there are more tests to come back in the lab and the unusual physiology parks has proved to have consequences not only for cognitive decline, but more for future Everest climbers directly.

exceptionally strong response to altitude Parks suggests that climbers could "overacclimatize" said Bailey, or themselves and others in danger by spending too much time at high altitude in order to an ascent. This goes against the prevailing wisdom that complete acclimatization is a must for any ascent without supplementary oxygen

And given the trappings of healthy parks, it is difficult to know the extent the problem could be :. How many climbers are already these symptoms without knowing it? And expected high altitude specialists test for this mountain? These are not the questions, the team supposed cause, but that does not mean they are unwelcome. "This is the dynamics of science," said Bailey. "You may come across some results ... which can be as deep as the original question you want to answer."

A previous encounter with a disease that occurs throughout Latin America could leave people more vulnerable to Zika . The anti-dengue virus antibodies, a relative of Zika, can interfere with the immune system to Zika and strengthen the ability of the virus to replicate, as the work in two independent laboratories. This may help explain why the complications of Zika virus infections were more severe in Central and South America than in previous outbreaks elsewhere.

In some regions of Brazil, as much as 0% of people carry antibodies against dengue. Dengue virus there are four types, have an unusual relationship with the immune system. Antibodies that develop after infection with one type does not protect against infection with another type. Instead, the antibodies may actually help the second virus invade certain immune system cells where the virus replicates easily, making the infection worse. The phenomenon is known as antibody-dependent enhancement (ADE), and it helps explain why the most serious cases of dengue, including a very dangerous condition called hemorrhagic dengue trend fever occur when a patient catches a second type of dengue .

scientists have questioned whether the Zika virus, which is quite close to dengue to blur the results of diagnostic tests that look for antibodies, could also be close enough to cause ADE. This could help explain why Zika, who has long been thought to cause only mild disease, has suddenly been blamed for causing symptoms much worse in Brazil and elsewhere, including birth defects in babies infected in the womb and temporary paralysis called Guillain-Barre syndrome.

the first support for the theory came from a paper published on the preprint server bioRxiv in April. Sharon Isern and Scott Michael of Florida Gulf Coast University in Fort Myers and colleagues reported that two grown antibody laboratory dengue and blood serum of patients with dengue (which contains antibodies) significantly stimulated virus replication Zika in laboratory cells.

Today, in an article published online in Nature Immunology , an independent group at Imperial College London reported similar results, showing that a number of different antibodies against the dengue virus respond to Zika, but not strongly enough to neutralize the virus. Instead, when the blood plasma of patients who had recovered dengue was added to cultures of cells infected with Zika, it increased the amount of virus in cultures by as much as 100 times.

The data is convincing, says Ernesto Marques, a public health expert at the University of Pittsburgh in Pennsylvania. But clinical and epidemiological studies need to confirm that the effect plays a role in patients. There are cases of congenital Zika syndrome in babies and mothers who do not have dengue antibodies, he notes, so although dengue antibody may increase the risk of a mother passing the virus to her fetus, antibodies are not essential to cause birth defects. Studies that look for antibodies against dengue among patients Zika are complicated by the similarity of the virus, says Gavin Screaton, an immunologist at Imperial College London and an author on the Nature Immunology paper. "We desperately need" blood tests that can easily distinguish whether a patient has antibodies against dengue, Zika, or both, he said.

Even if the results are confirmed, there are not many people who have already been infected with dengue can do to protect themselves, but reduce the risk of mosquito bites, eg using repellent . But these precautions are already recommended for everyone in affected countries Zika.